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Biomedical subjects

G L Klein

Publications and source records attributed to G L Klein.

90 records · Page 5Linked to original sources
PubMed1980

Bone disease associated with total parenteral nutrition.

An unusual metabolic bone disease which developed in 11 adults receiving total parenteral nutrition (TPN) for more than 3 months was characterised by the insidious onset of bone pain which became very severe and caused considerable disability. Serum levels of calcium, phosphorus, 25-hydroxy-vitamin D, and serum immunoreactive parathyroid hormone were normal. Patchy osteomalacia with impaired mineralisation and decreased bone turnover were seen on histomorphometric analysis of bone biopsy specimens. All patients receiving long-term TPN had hypercalciuria, but no biochemical features that distinguished patients with symptoms from those without. Skeletal symptoms generally resolved 1-2 months after stoppage of the TPN infusions, despite nutritional deterioration. The pathogenesis of this syndrome remains unknown.

Adult↗
PubMed1980

Monozygotic twins with Crohn's disease: a case report.

Twin brothers whose monozygosity was demonstrated by analysis of dermatoglyphic patterns, chromosome banding, HLA typing, and gene markers developed Crohn's disease within 8 mo of each other. Both had involvement of the terminal ileum, colon, and rectum, as well as arthritis. However, one had severe esophagitis and recurrent pancreatitis, and the other had severe arthritis and oral mucosal involvement. Both twins had manifestations controlled by parenteral nutrition. This report describes the similarities and differences in the complicated course of Crohn's disease in identical twins and demonstrates that while the development of Crohn's disease may be genetically influenced the site of gastrointestinal involvement is affected by other factors. This experience does not support previously held concepts of the role of genetics in the clinical manifestations of Crohn's disease.

Adolescent↗
PubMed1979

Nutritive value of elemental formula with reduced osmolality.

The osmolality of an elemental formula was reduced from 627 to 338 mOsm/kg H2O by replacing dextrose with corn syrup solids, reducing the content of casein hydrolysate, and replacing a portion of the medium-chain triglycerides with corn oil. In three convalescent malnourished infants, the protein quality of the formula was compared at isonitrogenous levels with that of a casein-sucrose-vegetable oil formula and was found to be at least as high: in all three nitrogen retention was higher than during a preceding casein period, and in one of the three it was also higher than during a following casein period. The levels of postprandial plasma amino acids suggested that threonine might be the first-limiting amino acid. Four severely malnourished infants received the formula as their only food during initial rehabilitation. The formula was well tolerated and supported satisfactory weight gain, linear growth, and serum protein regeneration.

Evaluation Studies as Topic↗
PubMed1978

Transient steatorrhea following episodes of mild diarrhea in early infancy.

Fecal fat excretion was studied after a mild episode of diarrhea in eight infants for whom adequate control data were available. Mean age of onset of diarrhea was 28 days. Duration of the episode, defined as the number of days until the infant was again feeding and libitum, averaged 5.1 days. Balance studies were carried out 3 to 13 days later. Mean fecal fat excretion rose from a prediarrhea value of 2.9 +/- 1.4 gm/day to 8.7 +/- 3.1 gm/day following diarrhea (P less than 0.001). Restudy of five infants one month later showed persistent steatorrhea in one. Mild transient steatorrhea may follow mild diarrhea in infancy and should be considered in infants who are slow to gain weight subsequent to an episode of diarrhea.

Animals↗
PubMedDate not supplied

Management of hymenoptera sting anaphylaxis: a preventive medicine survey.

The evaluation of aftercare instructions given to patients suffering from hymenoptera sting anaphylaxis was the objective of the study. Part of this evaluation included asking the physicians questions to examine the knowledge on which they based their aftercare instructions. Survey questionnaires were completed by 124 of 174 (71%) physicians who worked in an emergency department or urgent care center. Fifty-eight percent of the physicians never provided written avoidance instructions, 24% provided or prescribed anaphylaxis ID bracelets, 44% referred all of their patients to an allergist for further evaluation, and 73% reported prescribing an Epi-pen or Ana-kit to all hymenoptera sting anaphylaxis victims. Twenty-four percent of physicians did not know where to obtain anaphylaxis identification bracelets. This survey demonstrates that a substantial number of physicians practicing emergency medicine are not providing appropriate aftercare instructions to patients, and substantiates the need for educational efforts to increase the awareness of physicians concerning the implications of hymenoptera allergy and the value of proper preventive measures.

Anaphylaxis↗
PubMedDate not supplied

Elevated serum aluminum levels in severely burned patients who are receiving large quantities of albumin.

Aluminum contaminates various fluids that are used in intravenous therapy, and it is associated with bone disease and encephalopathy. Albumin is highly contaminated with aluminum, which is eliminated primarily by renal excretion. Patients with burns receive large quantities of albumin and have impaired renal function, which puts them at hypothetical risk for aluminum loading. To assess the risk of aluminum loading we analyzed sera from 12 patients with burns for aluminum concentrations. Serum aluminum concentration was elevated in 8 of the 12 patients, and levels were at or near toxicity in 3 of the 8. Serum aluminum and serum creatinine levels directly correlated, r = 0.71 and p less than 0.005. No relation was found between serum aluminum and amount of albumin received. However, patients with the highest serum aluminum levels were the most severely burned and none survived. Thus patients with burns who are receiving albumin are at risk for aluminum loading. Impaired renal function contributes to aluminum retention.

Adolescent↗
PubMedDate not supplied

Risk of aluminum accumulation in patients with burns and ways to reduce it.

Severely burned patients experience a bone lesion consisting of markedly reduced bone formation and evidence of decreased resportion. The cause of the lesion may be multifactorial, but aluminum loading, which also occurs in patients with burns, has been documented to produce this type of injury in both humans and animals. To assess the risk of aluminum loading with patients with burns, we analyzed fluids, creams, and medication used in the management of acute burn injury for aluminum content. These substances were classified according to route of administration: cutaneous, enteral, or parenteral, to assess the risk of aluminum loading. Cutaneous exposure to aluminum is greatest from baths, which may provide up to 8 mg aluminum. However, the dynamics of aluminum entry into the blood via a damaged skin barrier are unclear. Enteral exposure to aluminum is no greater than daily dietary exposure. Parenteral sources of aluminum, especially 25% human serum albumin and calcium gluconate, provide the most significant risk of loading because of direct introduction of aluminum into the circulation. Substitution with a different brand of albumin and calcium chloride can reduce the parenteral aluminum load by as much as 95% and minimize any role aluminum may play in the pathogenesis of this bone lesion.

Administration, Topical↗
PubMedDate not supplied

Burn-associated bone disease in sheep: roles of immobilization and endogenous corticosteroids.

To determine the role of immobilization in the pathogenesis of burn-associated bone disease, we selected the sheep as a model to study the effects of burn injury compared with a sham-burned control group. Seven of the sheep were subjected to controlled 40% flame burn, and seven underwent anesthesia with arterial and venous cannulation but without burn. After labeling newly formed bone with tetracycline and calcein, the sheep were killed 2 weeks after burn or sham burn, and the iliac crest and lumbar vertebrae were analyzed for histomorphometry. Analysis failed to demonstrate a significant reduction of bone formation rate in the burned sheep. Osteoid area and surface and osteoblast surface, which correlated significantly with bone formation rate (r = 0.49, p < 0.025), were reduced in the burned sheep. Results suggest that immobilization may play a primary role in the pathogenesis of burn-associated bone disease, but the presence of differences in other histomorphometric features indicates the bone disease is multifactorial.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Aluminum does not accumulate in teenagers and adults on prolonged parenteral nutrition containing free amino acids.

Prolonged total parenteral nutrition (TPN) with solutions containing hydrolyzed casein has been associated with aluminum accumulation in patients with bone disease. We investigated the effects of free amino acids in TPN solution on plasma, urine, and bone aluminum in six patients, five of whom had symptoms of bone disease or documented demineralization. No evidence of aluminum accumulation was found. TPN with free amino acids, containing 42 micrograms aluminum per liter or less, does not lead to aluminum loading in adolescents or adults.

Adolescent↗
PubMedDate not supplied

Hepatic abnormalities associated with aluminum loading in piglets.

Cholestasis is a common complication of total parenteral nutrition (TPN) in infants. A contributing factor to the hepatic dysfunction may be a contaminant of the TPN solution, such as aluminum, that accumulates in liver and may act as a hepatotoxin. To study the hepatic effects of aluminum, growing piglets were given daily intravenous injections of aluminum, 1.5 mg/kg, for 50 days; pair-fed controls were given heparinized saline. At sacrifice, liver and serum were obtained. Liver was analyzed for histopathology and for aluminum content and localization. The hepatocyte lysosomes of the experimental group showed aluminum peaks by x-ray microanalysis, whereas the control group did not. No differences in ultrastructure were noted between the two groups when examined by electron microscopy. Mean serum total bile acid levels (27.8 +/- 15.9 SD vs 6.3 +/- 1.5 mumol/liter, p less than 0.05), mean alkaline phosphatase (309 +/- 108 vs 180 +/- 27 IU/liter, p = NS), and mean hepatic copper content (24.8 +/- 4.5 vs 14.4 +/- micrograms/g dry weight, p less than 0.01), were elevated in the aluminum-loaded piglets, indicating that cholestasis may have been produced. Also, a small but significant reduction in serum levels of 25 hydroxy-vitamin D was found in the aluminum-loaded piglets, suggesting that vitamin D hydroxylation may be impaired. Inasmuch as lysosomal contents are excreted into the bile, aluminum accumulation in lysosomes may alter lysosomal function and possibly affect bile flow or content.

Aluminum↗
PubMedDate not supplied

Aluminum in parenteral products: medical perspective on large and small volume parenterals.

Bone abnormalities may complicate parenteral nutrition (PN) therapy given to patients. Bone disease, manifested by reduced bone formation and demineralization in adults, and poor mineralization in infants, is associated with bone aluminum accumulation at the mineralizing surface. Aluminum was first shown to contaminate casein hydrolysate, the PN protein source. Substitution of amino acid solutions, low in aluminum, reduced bone aluminum and improved bone formation in adults. Aluminum also accumulates ten-fold in the bones of premature infants receiving chronic PN. Present sources of aluminum in PN are calcium and phosphate salts, albumin, and heparin. Although increased bone aluminum in infants is not proven to cause disease, use of deferoxamine in one infant produced hypocalcemia. This suggested that chelation of bone aluminum by deferoxamine increased bone calcium uptake. Thus aluminum in bone may impair bone calcium uptake and may contribute to the pathogenesis of PN-related bone disease in infants. Another complication of PN therapy in infants is cholestatic liver disease, manifested by reduced bile flow, and, occasionally, gallstones. Aluminum has been found to accumulate in the livers of these infants, and there is experimental evidence that aluminum can reduce bile flow both in rats and in piglets. Aluminum contamination of PN solutions puts infants at increased risk for complications of PN therapy; amounts of aluminum in PN solutions should therefore be minimized.

Adult↗